RNa extracted from Brca1 presence/absence mice livers and processed on Mouse Expression 430A chips and processed by the NIDDK microarray facility
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Age, Specimen part, Disease, Disease stage, Subject, Time
View SamplesThe research of maize freezing tolerance.
No associated publication
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Specimen part
View SamplesTick-borne flaviviruses (TBFVs) are ss(+)RNA viruses that cause febrile illnesses, which may progress to severe encephalitis and/or death in humans globally. 30—60% of people who recover from severe acute disease continue to suffer debilitating neurological sequelae due to viral persistence, neurological cell damage incurred during infection and/or host response, or a combination of these. When TBFVs infect mammalian cells in vitro, an acute phase characterized by dramatic apoptosis ensues and kills >95% of infected cells by day 5. Upon refreshing the cell growth medium, surviving cells repopulate and become persistently infected for extended periods of time. However, molecular mechanisms responsible for the initiation and maintenance of viral persistence in vivo and in vitro remain vague. We used unbiased deep sequencing of the HEK 293T cell transcriptome to determine the profiles of acutely infected cells at selected time points as well as of persistently infected cells. Many genes were significantly differentially expressed during the course of the acute phase, but 451 genes were significantly differentially expressed uniquely in persistently infected cells. Ingenuity Pathways Analysis of these genes suggested that the oncogenes AKT2 and ERBB2, which favor cell survival were up-regulated in persistently infected cells, whereas pro-apoptotic genes, such as Bad and IFN-ß1 were down-regulated. There was also an up-regulation of genes encoding antiviral cytokines, such as CCL5, TNF-a and CXCL10 during the acute phase, but these were relatively suppressed in persistently infected cells. Exogenous induction of apoptosis in persistently infected cells with chelerythrine chloride indicated that these cells were resistant to apoptosis in a dose-dependent manner. In summary, the transcriptome profiles of acutely and persistently infected HEK 293T cells are different and evasion of apoptosis is critical for the initiation of TBFV persistence. These results provide a basis for further studying the precise molecular mechanisms of TBFV persistence.
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View SamplesOverconsumption of high-fat diet (HFD) and sugar-sweetened beverages are risk factors for development of obesity, insulin resistance and fatty liver disease. To dissect mechanisms underlying this association, mice were fed chow or HFD with or without addition of fructose- or glucose-supplemented water. There were no physiological differences in mice supplemented with fructose or glucose on chow diet. Despite similar caloric intake, mice on HFD supplemented with fructose developed more pronounced obesity, glucose intolerance and hepatomegaly than glucose-supplemented mice. While both sugars increased Chrebp-?, fructose supplementation uniquely increased Srebp1c and downstream fatty acid synthesis genes resulting in reduced liver insulin signaling, whereas glucose enhanced total Chrebp expression and triglyceride synthesis but was associated with improved hepatic insulin signaling. Metabolomic and RNA sequence analysis confirmed dichotomous effects of fructose and glucose supplementation on liver metabolism in spite of inducing similar amount of hepatic lipid accumulation. Ketohexokinase, the first enzyme of fructose metabolism, was increased in fructose-fed mice and in obese adolescents with steatohepatitis. Knockdown of ketohexokinase-C in liver improved hepatic steatosis and glucose tolerance in fructose-supplemented mice. Thus, fructose is a component of dietary sugar that is uniquely associated with poor metabolic outcomes, while increased glucose intake may be protective.
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Sex, Age, Specimen part, Cell line
View SamplesBy using DREADD technology, we found that activating Gi signaling in hepatocytes promotes hepatic glucose production. While we demonstrated that intact JNK signaling is required for maximal glucose output after stimulation of hepatic Gi signaling, other pathways may also contribute to this response. To obtain information about such non-JNK-dependent pathways, we studied changes in hepatic gene expression in an unbiased fashion using RNA-seq analysis. In this study, we used a viral delivery strategy to selectivity express a Gi-coupled DREADD (full name: hM4Di) in mouse hepatocytes (Hep-Di mice). We prepared liver RNA from Hep-Di mice 30 min after injection with either CNO (10 mg/kg i.p.) or saline (control) and then subjected these RNA samples to RNA-seq analysis.
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Sex, Age, Specimen part, Cell line
View SamplesSex condition has been demonstrated to alter meat quality and sex is a major factor that affects the fatty acid composition of lipids of carcass dissectible or intramuscular depot fats. But the possible genetic molecular mechanism of gender causing meat quality differences is not well defined. Qinchuan cattle, Qinghai yak and Guangxi buffalo are three typical indigenous species of cattle in China. Obivious differences of meat quality exist among the three species of cattle. Few studies have been conducted to elucidate the muscle tissue expression of genes involved in pathways and mechanisms leading to meat quality differences beyond the phenotype properties of beef.
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Sex, Age, Specimen part
View SamplesOverexpression of the novel Arabidopsis gene At5g02890
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Specimen part
View SamplesTranscriptomic analysis of BnLATE-regulated pathways to investigate the genome-wide effects of BnLATE overexpression on transcription
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Specimen part
View SamplesWe measured mRNA abundance in the embryogenic tissue of 150 recombinant Steptoe x Morex doubled-haploid lines (no replicates) and in parental genotypes, Steptoe and Morex, 3 replicates each, total 156 chips.
SFP genotyping from affymetrix arrays is robust but largely detects cis-acting expression regulators.
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Age, Specimen part, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
The response and recovery of the Arabidopsis thaliana transcriptome to phosphate starvation.
Age, Specimen part, Treatment
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